Lawaetz Andreas C, Almstrup Kristian
Biomol Concepts. 2015 Jun;6(3):219-27. doi: 10.1515/bmc-2015-0006.
Testicular germ cell cancer manifests mainly in young adults as a seminoma or non-seminoma. The solid tumors are preceded by the presence of a non-invasive precursor cell, the carcinoma in situ cell (CIS), which shows great similarity to fetal germ cells. It is therefore hypothesized that the CIS cell is a fetal germ cell that has been arrested during development due to testicular dysgenesis. CIS cells retain a fetal and open chromatin structure, and recently several epigenetic modifiers have been suggested to be involved in testicular dysgenesis in mice. We here review the possible involvement of epigenetic modifiers with a focus on jumonji C enzymes in the development of testicular dysgenesis and germ cell cancer in men.
睾丸生殖细胞癌主要在年轻成年人中表现为精原细胞瘤或非精原细胞瘤。在实体瘤出现之前,存在一种非侵袭性的前体细胞,即原位癌细胞(CIS),它与胎儿生殖细胞具有高度相似性。因此,有人推测CIS细胞是由于睾丸发育异常而在发育过程中停滞的胎儿生殖细胞。CIS细胞保留了胎儿期开放的染色质结构,最近有几种表观遗传修饰因子被认为与小鼠的睾丸发育异常有关。我们在此综述表观遗传修饰因子,特别是聚焦于Jumonji C酶在男性睾丸发育异常和生殖细胞癌发生过程中的可能作用。